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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endocrine responses to the serotonin (5-HT) 5-HT1C/5-HT2 agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) were utilised to evaluate cocaine-induced alterations in postsynaptic 5-HT receptor function. Rats received cocaine HCl (0, 5 or 15 mg/kg i.p.) twice daily for 7 days. Effects of DOI (0, 0.5, 2 or 10 mg/kg i.p.) on plasma adrenocorticotropic hormone (ACTH), corticosterone, prolactin, oxytocin and renin concentrations were assessed 42 h after the final cocaine injection. DOI dose dependently increased the plasma concentrations of each hormone. Cocaine potentiated the DOI-induced elevations of plasma ACTH, corticosterone and prolactin concentrations. In contrast, the oxytocin response was reduced, and the renin response was unaltered by cocaine exposure. The data suggest that 5-HT2 receptor-mediated responses for ACTH, corticosterone and prolactin secretion become supersensitive following repeated cocaine. In contrast, the 5-HT2 receptor-mediated response for oxytocin secretion is subsensitive. The cocaine-induced changes in postsynaptic 5-HT receptor function are likely a consequence of deficits in the function of 5-HT nerve terminals, that we have documented previously.
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PMID:Repeated cocaine modifies the neuroendocrine responses to the 5-HT1C/5-HT2 receptor agonist DOI. 133 68

Cocaine use in pregnancy is associated with a premature labor rate as high as 50%, but little is known about its effect on uterine contractility. To determine whether cocaine directly augments pregnant uterus contractility, uterine strips from 27-day pregnant New Zealand White rabbits (term, 31 days) were exposed to cocaine alone (30 mumol/L) or cocaine plus epinephrine (10(-9) to 10(-5) mol/L) or oxytocin (10(-10) to 10(-6) mol/L). Cocaine alone produced no contractions, but increased the epinephrine sensitivity by 51% and the maximal response by 33%. When beta-adrenoceptors were blocked with DL-propranolol (2 mumol/L), the contractile response to epinephrine was increased, and cocaine's effect was blocked. In the presence of the stereoisomer D-propranolol (2 mumol/L) with no beta-adrenergic antagonist activity, the contractile response to epinephrine was unchanged, but the effect of cocaine was still blocked. We conclude that cocaine directly augments the alpha-adrenergic contractile response of the pregnant rabbit uterus by a mechanism that is blocked by the non-beta-adrenergic effects of propranolol.
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PMID:Cocaine directly augments the alpha-adrenergic contractile response of the pregnant rabbit uterus. 167 Sep 9

Although cocaine abuse during human pregnancy is associated with an increased incidence of preterm labor, there are few reports on the effects of cocaine on myometrial activity during pregnancy in experimental animals. Cocaine (0.5, 1, or 2 mg/kg) or vehicle was randomly administered intravenously to 15 pregnant ewes between 124-146 days' gestation (term is 147 days). Neither cocaine nor vehicle administration altered total myometrial electromyographic activity from pre-dose levels 1 or 6 hours after administration. Maternal arterial plasma oxytocin did not change during the study. Using a positive control, we confirmed observations of other investigators that administration of 2 mg/kg cocaine significantly increases maternal arterial blood pressure. The results indicate that cocaine does not stimulate myometrial contractility significantly in late pregnancy in sheep.
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PMID:Lack of effect of maternal cocaine administration on myometrial electromyogram and maternal plasma oxytocin concentrations in pregnant sheep at 124-146 days' gestational age. 172 92

The effects of pimozide, a dopamine-receptor blocker and oxytocin, a neurohypophyseal neuropeptide were investigated in mice on the cocaine-induced exploratory hyperactivity. The action of oxytocin on changes of dopaminergic neurotransmission induced by cocaine was also measured. Cocaine-induced exploratory hyperactivity could be blocked by pimozide (1 mg kg-1, s.c.). Oxytocin (0.05-1.0 micrograms) inhibited the cocaine-induced hyperactivity in an U-shaped dose-response manner. In the nucleus accumbens, oxytocin antagonized the increased dopamine disappearance, elicited by cocaine, but not in the nucleus caudatus. The data suggest that oxytocin may influence the behavioural effect of cocaine by modulating dopaminergic neurotransmission in mesolimbic dopaminergic terminal region of the brain.
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PMID:Oxytocin attenuates the cocaine-induced exploratory hyperactivity in mice. 198 56

Cocaine is a widely used drug of abuse. One of the characteristic effects of this stimulant drug in the CNS of mice is the induction of motor hyperactivity. It was demonstrated that cocaine-induced motor hyperactivity could be blocked by pimozide, a dopamine receptor blocker, suggesting that dopamine was involved in cocaine-induced hyperactivity. Oxytocin, a neurohypophyseal neuropeptide, also partially antagonized cocaine-induced motor hyperactivity. Moreover, oxytocin antagonized the increased utilization of dopamine, elicited by cocaine in the nucleus accumbens. The data suggest that oxytocin may influence the behavioural effects of cocaine by affecting dopaminergic neurotransmission in some regions of the brain.
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PMID:The role of oxytocin-dopamine interactions in cocaine-induced locomotor hyperactivity. 216 Jun 23

We examined the effects of an acute cocaine treatment on oxytocin levels in the whole hippocampus, ventral tegmental area (VTA) and amygdala in ovariectomized rats pretreated with 10 micrograms estradiol benzoate. Cocaine treatment significantly reduced oxytocin levels both in picograms/area and picograms/mg wet weight in the hippocampus but had no significant effect on levels in the VTA and amygdala. These data represent the first evidence for the reduction of oxytocin levels as a result of an acute cocaine treatment.
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PMID:Acute cocaine treatment decreases oxytocin levels in the rat hippocampus. 847 35

We examined the effects of gestational cocaine treatment on oxytocin levels in the whole hippocampus (HIP), ventral tegmental area (VTA), medial preoptic area (MPOA) and amygdala (AMY) in rat dams on postpartum days (PPDs) 1 and 2. Cocaine treatment significantly reduced oxytocin levels in the MPOA within 12-16 h of delivery (PPD 1), but had no significant effect on the other brain areas. Oxytocin was significantly reduced in the HIP and VTA but not in the AMY or MPOA on PPD 2. These data provide the first evidence for the reduction of oxytocin levels in the VTA, HIP and MPOA as a result of gestational cocaine treatment.
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PMID:Chronic gestational cocaine treatment decreases oxytocin levels in the medial preoptic area, ventral tegmental area and hippocampus in Sprague-Dawley rats. 941 20

Cocaine and amphetamine regulated transcript (CART) has been identified as one of the most abundant mRNAs in the rat hypothalamus. The objective of the present study was to elucidate the distribution of CART peptide immunoreactive (CARTir) neurons in the monkey hypothalamus and characterize their ultrastructural features and synaptic connections in the paraventricular nucleus (PVN). CARTir neurons were particularly abundant in the PVN, supraoptic nucleus (SON), infundibular nucleus, and premammillary nucleus, whereas the anterior, lateral, and posterior hypothalamic areas as well as the posterior nucleus displayed moderate immunoreactivity. Dense bundles of CARTir fibers exited the PVN and SON and followed a trajectory to the infundibulum similar to that previously shown for vasopressin and oxytocin fibers. The posterior pituitary was densely packed with large CARTir varicosities which, in some cases, were apposed to labeled pituicytes. The external/palisade zone of the median eminence contained rich plexuses of small CARTir varicose fibers, and the internal/fibrous zone was enriched in large axon-like processes. Electron microscope analysis of the PVN revealed (1) that CART peptide immunoreactivity is found in neurosecretory and non-neurosecretory neurons contacted predominantly by unlabelled terminals forming asymmetric synapses, (2) that CARTir terminals resemble glutamatergic and/or noradrenergic boutons and form asymmetric synapses with non-neurosecretory dendrites, and (3) that neuropeptide Y (NPY)-containing terminals are apposed to CARTir neurons in the medial part of the nucleus. In conclusion, our findings demonstrate that CART peptide is abundant in neuronal perikarya and axon terminals throughout the monkey hypothalamus and along the hypothalamopituitary axis. This strengthens the idea that CART peptides may act as putative neurotansmitters/neuromodulators that mediate various neuroendocrine and autonomic functions in primates.
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PMID:CART peptide immunoreactivity in the hypothalamus and pituitary in monkeys: analysis of ultrastructural features and synaptic connections in the paraventricular nucleus. 1060 89

Chronic gestational cocaine administration has been correlated with high levels of postpartum maternal aggression towards intruders and altered levels of oxytocin in the amygdala. Cocaine may alter both oxytocin and maternal aggression either directly or indirectly through changes in monoamine levels in relevant brain regions. In this study, pregnant female rats were randomly assigned to one of four groups; three cocaine dose groups (7.5, 15 or 30 mg/kg), or a saline-treated group (0.9% normal saline) and given subcutaneous injections twice daily (total volume 2 ml/kg) throughout gestation. Behavioral responses to an inanimate object placed in the homecage were assessed on Postpartum Day (PPD) 6. Immediately following testing, animals were sacrificed and four brain regions implicated in maternal/aggressive behavior (medial preoptic area [MPOA], ventral tegmental area [VTA], hippocampus, and amygdala) were removed for monoamine level analyses using high-performance liquid chromatography. Dams given 30 mg/kg cocaine throughout gestation had significantly higher levels of dopamine (DA) and nonsignificantly elevated serotonin (5-HT) levels relative to saline-treated controls. These dams also exhibited higher frequencies of defensive behavior toward an inanimate object compared to saline-treated controls. Potential mechanisms mediating cocaine-induced increases in responding are proposed.
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PMID:Effects of chronic cocaine on monoamine levels in discrete brain structures of lactating rat dams. 1247 66

Cocaine administered chronically throughout gestation has been correlated with deficits in maternal behavior, increased maternal aggressive behavior and decreased oxytocin levels in rats. In addition to its effects on oxytocin levels, cocaine is a potent serotonergic, dopaminergic and noradrenergic reuptake inhibitor. Alterations in the dopaminergic and serotonergic systems have been suggested as possibly having a role in cocaine-induced maternal aggression. This study was in part, an attempt to understand some of the mechanisms by which cocaine increases postpartum aggression, particularly as they relate to changes in the oxytocin system. Oxytocin receptor number and binding affinity in the medial preoptic area of the hypothalamus, ventral tegmental area, hippocampus and amygdala were determined for lactating rat dams on postpartum day 6 (PPD 6) that were gestationally treated with cocaine, fluoxetine, saline or an amfonelic acid/fluoxetine drug combination. Cocaine and fluoxetine treatment both resulted in a significant up-regulation of oxytocin receptor number and lower receptor affinity in the amygdala of lactating rat dams compared to saline controls and the amfonelic acid/fluoxetine combination treatment group. Cocaine treatment also resulted in a significant down-regulation of oxytocin receptors in the medial preoptic area and both cocaine and fluoxetine treated dams had the highest affinity for oxytocin receptors in this brain region. Results of the present study support previous data indicating that alterations in oxytocinergic and perhaps serotonergic system dynamics in the amygdala may play a role in cocaine-induced postpartum aggression.
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PMID:Gestational treatment with cocaine and fluoxetine alters oxytocin receptor number and binding affinity in lactating rat dams. 1538 Aug 31


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